Relatively minor falls or seemingly unimportant incidents, often not recalled, may cause significant trauma in the elderly. Injuries may be missed or underestimated.
Ageing leads to progressive functional decline and reduced physiological reserve. Frailty is a risk factor for ongoing complications and slower recovery.
Reduced compliance and impaired ventricular diastolic filling, lead to lower cardiac output reserve. Tachycardia exacerbates the decrease in cardiac output.
Downregulation of beta-adrenoceptors leads to reduced response to inotropic drugs and a profound reduction in cardiac output on induction of anaesthesia.
Higher resting diastolic and systolic blood pressures. Hypovolaemic shock may be relatively masked with hypotension representing a greater blood loss than in a normotensive individual.
Arrhythmias are more common due to fibrosis of cardiac conducting tissue. Atrial fibrillation (AF) is common. Sympathetic stimulation increases the risk of arrhythmias and both lead to reduced cardiac output and compromised myocardial blood supply. Furthermore AF increases the risk of venous thromboembolism post-trauma.
Pulse pressure is widened due to atherosclerosis of blood vessels. This can mask the narrowing of pulse pressure that results in hypovolaemic shock.
Coronary blood flow is reduced due to degenerative calcification, thickening of the tunica intima and atherosclerosis. This means that in the face of hypotension, cardiac ischaemia is more likely than in healthy individuals.
Desensitisation of baroreceptors in the carotid sinuses and aortic arch means that reflex responses to hypotension are reduced. Induction of anaesthesia, particularly in the face of hypotension, can induce profound hypotension.
Normal responses to hypovolaemia may be masked by drugs: beta blockers may prevent tachycardia in response to hypovolaemia; antihypertensives may exacerbate hypotension.
Structural changes in the airways with ageing lead to an increased tendency for airway collapse during sleep and anaesthesia. These changes also increase airway compliance, leading to compression of small airways and closure during expiration resulting in air trapping. The residual volume increases, as does the functional residual capacity (larger oxygen reservoir if full pre-oxygenation is possible).
Respiratory muscles are weaker in the elderly.
Volume of the pulmonary vasculature decreases and the pulmonary vascular resistance increases significantly (approximately 75%) as does pulmonary artery pressure (25%).
Reduced alveolar surface area as a result of small airway dilatation leads to a worsening of gas exchange.
FVC and FEV1 are reduced.
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